Impact of inhalation exposure to cigarette smoke on the pathogenesis of pulmonary hypertension primed by monocrotaline in rats.

arteriolar hypertrophy cigarette smoke monocrotaline pulmonary hypertension smoking

Journal

Journal of applied toxicology : JAT
ISSN: 1099-1263
Titre abrégé: J Appl Toxicol
Pays: England
ID NLM: 8109495

Informations de publication

Date de publication:
24 Oct 2023
Historique:
revised: 26 09 2023
received: 03 07 2023
accepted: 26 09 2023
medline: 25 10 2023
pubmed: 25 10 2023
entrez: 25 10 2023
Statut: aheadofprint

Résumé

Extensive, long-term exposure to cigarette smoke (CS) was recently suggested to be a risk factor for pulmonary hypertension, although further validation is required. The vascular effects of CS share similarities with the etiology of pulmonary hypertension, including vascular inflammation and remodeling. Thus, we examined the influence of CS exposure on the pathogenesis of monocrotaline (MCT)-induced pulmonary hypertension, hypothesizing that smoking might accelerate the development of primed pulmonary hypertension. CS was generated from 3R4F reference cigarettes, and rats were exposed to CS by inhalation at total particulate matter concentrations of 100-300 μg/L for 4 h/day, 7 days/week for 4 weeks. Following 1 week of initial exposure, rats received 60 mg/kg MCT and were sacrificed and analyzed after an additional 3 weeks of exposure. MCT induced hypertrophy in pulmonary arterioles and increased the Fulton index, a measure of right ventricular hypertrophy. Additional CS exposure exacerbated arteriolar hypertrophy but did not further elevate the Fulton index. No significant alterations were observed in levels of endothelin-1 and vascular endothelial growth factor, or in hematological and serum biochemical parameters. Short-term inhalation exposure to CS exacerbated arteriolar hypertrophy in the lung, although this effect did not directly aggravate the overworked heart under the current experimental conditions.

Identifiants

pubmed: 37876240
doi: 10.1002/jat.4555
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Ministry of Food and Drug Safety
ID : 21203MFDS318
Organisme : National Research Foundation of Korea
ID : 2022R1A2C2007171
Organisme : National Research Foundation of Korea
ID : NRF-2018R1A5A2023127
Organisme : Dongguk University Research Fund of 2022
ID : S-2022-G0001-00132
Organisme : Ministry of Education

Informations de copyright

© 2023 John Wiley & Sons Ltd.

Références

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Auteurs

Jung-Min Park (JM)

BK21 FOUR Team and Integrated Research Institute for Drug Development, College of Pharmacy, Dongguk University, Goyang-si, Gyeonggi-do, Republic of Korea.

Yoon-Seok Seo (YS)

BK21 FOUR Team and Integrated Research Institute for Drug Development, College of Pharmacy, Dongguk University, Goyang-si, Gyeonggi-do, Republic of Korea.

Sung-Hwan Kim (SH)

Inhalation Toxicology Research Group, Korea Institute of Toxicology, Jeongeup-si, Jeollabuk-do, Republic of Korea.

Hyeon-Young Kim (HY)

Inhalation Toxicology Research Group, Korea Institute of Toxicology, Jeongeup-si, Jeollabuk-do, Republic of Korea.

Min-Seok Kim (MS)

Inhalation Toxicology Research Group, Korea Institute of Toxicology, Jeongeup-si, Jeollabuk-do, Republic of Korea.

Moo-Yeol Lee (MY)

BK21 FOUR Team and Integrated Research Institute for Drug Development, College of Pharmacy, Dongguk University, Goyang-si, Gyeonggi-do, Republic of Korea.

Classifications MeSH